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Patient Care

Differential Diagnosis: Bell’s Palsy vs. Stroke

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You and your partner arrive at a private residence after being dispatched for a 60-year-old male experiencing a possible stroke. The patient’s concerned wife greets you at the door. You approach the patient and begin your primary survey as your partner obtains the patient’s medical history from the wife. The patient appears to be awake and oriented without airway, breathing or circulatory compromise.

As you continue your assessment, you note obvious slurring of speech and facial drooping on the left side, but there does not appear to be any noticeable arm drift. The patient’s pupils are equal, round and reactive to light, but you notice he seems to be having trouble closing his left eye. His pulse rate is 100 (strong and regular), and he is breathing 15 times a minute without effort. His blood pressure 156/86, breath sounds clear throughout, and blood glucose 90 mg/dL.

The patient says his symptoms started approximately an hour ago while he watched television. He denies having a headache or any other symptoms. The patient’s wife shares that he has a history of hypertension and takes hydrochlorothiazide as prescribed. She adds he’s been taking an over-the-counter cold medication for the past three days.

You and your partner promptly load the patient onto your stretcher and expedite transport to the local stroke center. You continue to monitor the patient en route and notify the emergency department that you’ll be arriving in 15 minutes with a stroke alert. Upon arrival you give a verbal report to the attending physician while the nurse and her team prepare the patient for a CT scan.

Later in the evening you transport another patient to the same ED and inquire about the stroke patient. The nurse tells you he was discharged about an hour after arrival with a diagnosis of Bell’s palsy. You feel an immediate sense of frustration. You were confident the patient was having a stroke and wonder if you missed something. On your way back to the station, you search the Web from your smartphone to refresh yourself on Bell’s palsy.

Background

Bell’s palsy is a self-limiting neurologic condition named after Sir Charles Bell, a surgeon in the British army who served at the Battle of Waterloo. Bell later went on to identify several notable connections of the spinal and cranial nerves. Among these findings was that lesion of the seventh cranial nerve results in facial paralysis.1

Bell’s palsy is among the most common causes of unilateral facial paresis (weakness) or paralysis, second only to stroke.2 Often considered a diagnosis of exclusion, Bell’s palsy is the most common diagnosis among patients who experience unilateral facial nerve paresis or paralysis of unknown origin.3 There are approximately 40,000 new cases annually in the United States, which can affect one out of every 60–70 people during a lifetime.2 This condition occurs across all age groups, genders and races. Prevalence increases with age, third-trimester pregnancy and diabetes.4,5 Other causes of facial paralysis include parotid tumors, zoster, sarcoidosis and Lyme disease.3

Patients experiencing Bell’s palsy might believe they are experiencing a stroke.6 For this reason they will often call EMS. Stroke can be a life-threatening condition that requires time-sensitive and invasive treatment regimens. However, Bell’s palsy is not life-threatening; up to 90% of patients may have complete recovery.7

EMTs and paramedics are taught to utilize a stroke scale or other assessment tool when assessing a suspected stroke patient. These tools typically evaluate three areas: facial symmetry, speech and extremity strength. While tools such as the Cincinnati Prehospital Stroke Scale only require the presence of a single positive finding (e.g., facial drooping) to be suggestive of stroke,8 one should not automatically assume that patients with unilateral facial asymmetry and slurred speech are always suffering a stroke. Just as there are risks of undertriage for patients who are potentially experiencing a stroke, potential risks of overtriage include heightened patient anxiety, operational dangers of transport using lights and sirens, and unnecessary use of scarce healthcare resources. For this reason, EMS personnel should develop a fundamental awareness of the presenting signs and symptoms associated with Bell’s palsy.

Pathophysiology

Bell’s palsy results from inflammation of the facial nerve, cranial nerve VII.9 This nerve, with its various branches, consists of roughly 10,000 neurons.10 The branches of the facial nerve are responsible for motor and sensory functions of the tongue, mouth, eyelids, cheeks and tear glands. Functions of cranial nerve VII include blinking, smiling, frowning, taste, lacrimation and salivation.3 Bell’s palsy may affect any of these functions. The facial nerve traverses the temporal bone through a narrow z-shaped pathway known as the fallopian canal. Space limitations within this canal mean the section of the facial nerve passing through it is subject to impingement in the presence of inflammation.10

The nerve becomes edematous secondary to inflammation, which creates a circumferential impingement as it traverses approximately 3 centimeters through the fallopian canal. The circumferential pressure exerted by the edema limits the blood flow, causing the nerve to become ischemic, resulting in unilateral facial paresis or paralysis.9 Long-term impingement may lead to permanent damage of the nerve and nonreturn of motor and sensory functions.2

Researchers have not been able to isolate the exact cause of Bell’s palsy.3 However, research has shown an association with activation of the herpes simplex virus type 1.9 Studies of both serologic analysis and autopsy findings relate the herpes simplex virus type 1 (HSV-1) and varicella zoster virus with Bell’s palsy patients.11 HSV-1 is the virus responsible for causing the cold sore.5 According to the National Institute of Allergy and Infectious Diseases, the varicella zoster virus is essentially the same virus that causes chicken pox and shingles.12 Other possible causes of Bell’s palsy may include autoimmune disorders, stress and vascular ischemia.6

Assessment

Patients with Bell’s palsy often present with a sudden onset of strokelike symptoms, including unilateral facial paralysis accompanied with loss of blink control on the affected side, decreased tearing and drooping of the mouth to the affected side.13 Other common signs and symptoms that may present within 48 hours of onset are altered sense of taste, slurring of speech, drooling, pain in or behind the ear and sound hypersensitivity on the side of paralysis.4,6,7,9 Bilateral symptoms are rarely seen, and their presence should lead the EMS provider to suspect other causes.2

Although stroke patients present with some of the same symptoms, they typically exhibit additional signs and symptoms not associated with Bell’s palsy (Table 1). Examples of these include changes in level of consciousness, dizziness, loss of coordination, seizure activity, changes in vision, and motor and/or sensory deficits in one or more extremities.14 Moreover, patients experiencing stroke do not typically present with forehead or eyelid weakness. Unlike a patient experiencing Bell’s palsy, patients experiencing a stroke will often retain the ability to blink with both eyes and furrow their brow.9

Bell’s palsy does not typically present with life-threatening conditions that need to be managed during the primary assessment. During the secondary assessment, focus your history and physical exam on evaluating specific complaints such as slurred speech or inability to blink. The provider should examine the area for trauma and complete a detailed neurological assessment.15 The neurological assessment should include level of consciousness, stroke scale evaluation, pupillary response and extremity evaluation. A more detailed cranial nerve assessment may also be included during the secondary assessment (see www.emsworld.com/11245200).

Past and current medical histories are also essential in the evaluation process. While Bell’s palsy can occur in men, women and children, it is most common among patients 15–45, diabetics, patients with upper respiratory infections, those with compromised immune systems, and during pregnancy.3 The history-gathering process should use the OPQRST mnemonic to assist in determining onset and rule out any previous trauma. Some patients may report a history of a recent viral infection, such as a cold, or express that they’ve been under stress recently.7

Management

Treatment of the Bell’s palsy patient is mostly supportive. Patients may need psychological support, especially if speech or facial expressions are altered.6 Special measures should be taken if the patient is unable to close their eyelid. Patch the affected eye to protect it from injury and help keep it moist.12 Consider obtaining a baseline blood glucose level in any patient with strokelike symptoms.4 Patients should be transported for more thorough evaluation, diagnosis and treatment.

Advanced Medical Management

In a comprehensive review of Bell’s palsy treatment, controversy still remains, with numerous studies evaluating the use of antivirals, corticosteroids, surgical decompression and combinations of therapy.16 Studies have shown that 80%–90% of patients recover fully within 3–6 months of the onset of symptoms with varying treatment regimens.5–7 Recovery rates as high as 66% have been seen in patients not receiving treatment;4 however, this should not undermine the importance of conducting a thorough evaluation of your patient.

Evidence from most studies indicates that the best results are achieved with a combination of corticosteroids, such as prednisone, and an antiviral, such as acyclovir, if started within 72 hours of the onset of symptoms. A review of three randomized, controlled studies of patients receiving corticosteroids alone concluded that corticosteroid treatment did not demonstrate significant improvements in patient outcomes.17 In a retrospective study of almost 500 patients, those treated with acyclovir and prednisone had a 97.5% recovery rate, versus 88.6% for patients treated with prednisone alone.18 The best results occurred with a combined pharmacologic treatment of acyclovir and prednisone that was started within three days of the onset. A meta-analysis of Bell’s palsy outcomes concluded the evidence indicated slightly better outcomes when combining an antiviral with a corticosteroid versus prednisone alone.19

Other approaches to the treatment of Bell’s palsy include patching the affected eye and providing lubricating eyedrops if the patient is unable to blink.12 Patients may also be instructed to perform facial exercises such as puffing the cheeks out and raising the eyebrows.4 While it’s controversial and not proven to improve facial function, some patients may also be treated surgically with facial nerve decompression if pharmacologic therapy doesn’t improve facial paralysis.2,5

Conclusion

As a prehospital care provider, you are likely to encounter a patient who presents with complaints similar to those in the opening scenario. Approach the patient experiencing Bell’s palsy like any other medical patient, with a thorough assessment and history in order to draw a field impression and treatment plan. Bell’s palsy is considered a diagnosis of exclusion, so it’s important to think critically and consider all pertinent negatives. Pay special attention to protecting the affected eye if the patient is unable to blink and providing the patient with reassurance. Consult medical control if Bell’s palsy is suspected to avoid unnecessarily declaring a stroke alert, but if in doubt, err on the side of caution.

References

1. Bell’s Palsy Association. Sir Charles Bell: 1774–1842, http://bellspalsy.org.uk/charlesbell.htm.

2. Gilden DH. Clinical practice. Bell’s Palsy. N Eng J Med, 2004 Sep 23; 351(13): 1,323–31.

3. Baugh R, Basura G, Ishii L, et al. Clinical Practice Guideline Summary: Bell’s Palsy. AAO-HNS Bulletin, 2013 Nov, www.entnet.org/sites/www.emsworld.com/files/Bulletin_BellsExecSummary_Final_102313.pdf.

4. Ahmed A. When is facial paralysis Bell palsy? Current diagnosis and treatment. Cleve Clin J Med, 2005 May; 72(5): 398–401, 405.

5. Holten KB. How should we manage Bell’s palsy? J Fam Pract, 2004 Oct; 53(10): 797–8.

6. Piercy J. Bell’s palsy. BMJ, 2005 Jun 11; 330(7,504): 1,374.

7. Carlson DS, Pfadt E. When your patient has acute facial paralysis. Nursing, 2005 Apr; 35(4): 54–55.

8. Kothari RU, Pancioli A, Liu T, Brott T, Broderick J. Cincinnati Prehospital Stroke Scale: reproducibility and validity. Ann Emerg Med, 1999 Apr; 33(4): 373–8.

9. Frock TL, McCaffrey R. Postauricular pain with Bell’s palsy. Nurse Pract, 2005 Apr; 30(4): 58–61.

10. Patel AA. Facial Nerve Anatomy. Medscape, http://emedicine.medscape.com/article/835286-overview.

11. Gilbert SC. Bell’s palsy and herpesviruses. Herpes, 2002 Dec; 9(3): 70–3.

12. National Institute of Allergy and Infectious Diseases. Facts about shingles (herpes zoster), http://www.niaid.nih.gov/factsheets/shinglesFS.htm.

13. Ronthal M. Patient information: Bell’s palsy. UpToDate, http://patients.uptodate.com/print.asp?print=true&file=gen_hlth/2073.

14. Mayo Clinic. Stroke: Symptoms and Causes, www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/dxc-20117265.

15. Bledsoe BE, Porter RS, Cherry RA. Paramedic Care Principles & Practice, Vol. 2, p. 292. Upper Saddle River, NJ: Pearson Education, 2006.

16. Grogan PM, Gronseth GS. Practice parameter: Steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 2001 Apr 10; 56(7): 830–6.

17. Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev, 2004 Oct 18; (4):CD001942.

18. Hato N, Matsumoto S, Kisaki H, et al. Efficacy of early treatment of Bell’s palsy with oral acyclovir and prednisolone. Otol Neuroltol, 2003 Nov; 24(6): 948–51.

19. Numthavaj P, Thakkinstian A, Dejthevaporn C, Attia J. Corticosteroid and antiviral therapy for Bell’s palsy: a network meta-analysis. BMC Neurol, 2011 Jan 5; 11(1): 1–10.

Glen Mayhew, DHSc, NRP, has been actively engaged in the emergency services profession for more than 25 years. He is currently an associate professor and associate dean for institutional effectiveness at Jefferson College of Health Sciences in Roanoke, VA, where he previously served as associate dean for academic affairs, chair of the Community Health Sciences Department and director of the emergency services program. Contact him at grmayhew@jchs.edu.

Elliot Carhart, EdD, RRT, NRP, is an associate professor of emergency services at Jefferson College of Health Sciences in Roanoke, VA. He is an experienced clinician, educator, researcher and author. Carhart is an associate of the UCLA Prehospital Care Research Forum and a member of the Editorial Advisory Board for EMS World. Contact him at researchmedic@icloud.com.

 

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